Lipid peroxidation-associated oxidative stress during percutaneous transluminal coronary angioplasty in humans.

Animal studies suggest that myocardial ischemia/reperfusion causes oxidative stress. We, therefore, examined whether routinely performed percutaneous transluminal coronary angioplasty (PTCA) might be a human ischemia/reperfusion model for oxidative stress-induced lipid peroxidation. Fasting antecubital venous blood was sampled from 13 patients on the morning of PTCA, and 2 d after PTCA. Venous and coronary arterial blood were sampled just before and 10 min after the first balloon inflation. Samples were analyzed for plasma and LDL lipid hydroperoxide levels, in vitro oxidation of LDL, and LDL antioxidant levels. Lipid hydroperoxide levels in plasma and LDL remained unchanged throughout the study. During the first 10 min of PTCA, the lag time during oxidation of LDL in vitro did not change, but the maximum rate of oxidation decreased in venous and arterial samples (Wilcoxon signed rank test: p < .002). At the same time, total tocopherol levels in LDL significantly increased by 6.3% (p = .048) in arterial, but not in venous samples. Total carotenoid levels increased by 3.8% (p = .127) in arterial samples and decreased by 2.9% (p = .040) in venous samples. Forty hours after PTCA, LDL oxidation parameters and LDL antioxidant levels were similar to baseline, except for about 17% lower levels of delta-tocopherol (p = .037) and gamma-tocopherol (p = .014). Our results, therefore, do not support that PTCA in humans is associated with oxidative stress-induced lipid peroxidation.